Izumi K
Mouridai Clinic, Kanagawa, Japan.
Mater Med Pol. 1989 Jul-Sep;21(3):213-22.
Bigeminal rhythm due to reentrant ventricular extrasystoles coupled to either ventricular escape of varying aberrant conduction or atrio-ventricular (A-V) junctional escape in association with coexisting idioventricular rhythm and A-V junctional rhythm is presented (Case 1). Dual A-V pathways with longitudinal dissociation in the left bundle branch was presumed to be the mechanism. Generally, both ventricular and A-V junctional escapes were discharged and reset as a result of the retrograde concealed conduction of the reentrant ventricular extrasystoles and the arrhythmia was thought to represent a variant of parasystole. Ventricular parasystole associated with ventricular bigeminy of bundle branch reentry, which was precipitated by hypokalemia during administration of a thiazide diuretic, was added for comparison (Case 2). In the latter, a reentrant ventricular extrasystole arising from the left anterior fascicle brought on and terminated ventricular parasystolic trigeminy and hexageminy of left posterior fascicular origin. Longitudinal dissociation with unidirectional block in the left posterior fascicle was presumed to be the mechanism. At times intermittent ventricular extrasystoles with broad and notched QRS in leads II and III initiated recurrent runs of ventricular bigeminy of varying bundle branch reentry.
本文介绍了一例（病例1）因折返性室性期前收缩与不同程度异常传导的心室逸搏或房室交界区逸搏相关联，同时并存心室自身节律和房室交界区节律而导致的二联律。推测机制为左束支存在纵向分离的双房室传导通路。通常，折返性室性期前收缩的逆行隐匿性传导会使心室和房室交界区逸搏均发放并重置，该心律失常被认为是并行心律的一种变异形式。为作比较，还补充了一例（病例2）因噻嗪类利尿剂治疗期间低钾血症诱发的、与束支折返性室性二联律相关的心室并行心律。在后者中，起源于左前分支的折返性室性期前收缩引发并终止了起源于左后分支的心室并行心律性三联律和六联律。推测机制为左后分支存在单向阻滞的纵向分离。有时，II导联和III导联出现宽大且有切迹QRS波的间歇性室性期前收缩会引发不同束支折返性室性二联律的反复发作。
